Clinical depression is marked prominently by symptoms of dysphoric mood often accompanied by anxiety, decreased interest in normal activities, work productivity, social interactions, and--in the extreme--a sense that life is not worth living, even leading to suicidal ideation and behavior. Depending on the depressive subtype, distinct sets of neurovegetative symptoms are apparent. "Classical" (melancholic) depressive disorders are marked by insomnia, reduced appetite and weight loss, and agitated behavior. By contrast, "atypical" depressive disorders--which are the present focus--are marked by continual fatigue, increased need for sleep (often with difficulty awakening), and increased appetite (often for carbohydrate-rich foods) and weight gain.
According to the official diagnostic classification of the American Psychiatric Association, disorders relevant to this application include Major Depressive Disorder (MDD, in which normal mood, or euthymia, is present outside the depressive episodes), Bipolar Disorders (in which mania or hypomania is sometimes present outside the depressive episodes), and "Not Otherwise Specified" disorders (NOS, in which depressive symptoms are clinically significant but do not meet severity criteria for MDD). Secondarily, these disorders may be further described as showing melancholic or atypical features, and as occurring in a seasonal pattern. These secondary descriptions do not define separate disorders, but rather clusters of specific symptoms and temporal course of clinical presentation.
Furthermore, clinical observation clearly shows individuals with neurovegetative disorders (of fatigability, hypersomnia and hyperphagia) that exist without depressed mood and yet are responsive to treatment interventions which are specifically active in atypical depressive disorders. Indeed, it has been noted that the onset of atypical depressive disorders can be initially detected in the emergence of the neurovegetative symptoms, with appearance of depressed mood occurring at a later stage.
It is now well acknowledged that the incidence of certain depressive disorders is not spontaneous or random, but is reliably triggered by external environmental factors. In one model, depressive disorders with seasonal pattern [which are also referred to outside the official diagnostic classification scheme as seasonal affective disorders (SAD)] are triggered by decreased environmental light exposure as the natural photoperiod contracts in autumn at northerly latitudes (winter depression) or, alternatively, by high temperature and humidity in summer (summer depression, in which a classical depressive profile is expressed). Atypical neurovegetative symptoms are hallmarks of winter depression; likewise, non-depressed individuals may show reliable cycles of wintertime fatigue, hypersomnia and hyperphagia (even including binge eating and bulimia nervosa, the latter being a diagnostically distinct eating disorder within the classification scheme of the American Psychiatric Association).
Although a majority of patients with winter depression regain normal levels of mood, energy, sleep and appetite in spring and summer, a distinct minority--estimated at one third of cases--becomes hypomanic, with exaggeratedly elevated (or "euphoric") mood and energy, often with racing thoughts, rapid speech and difficulty with concentration. Furthermore, the neurovegetative symptoms of winter are seen in the opposite extreme, with lower-than-normal appetite and greatly reduced sleep duration without loss of daytime energy.
Although, by formal definition, depressive disorders with seasonal pattern are characterized by normal mood, hypomania or mania outside the depressive episode, a large number of patients with chronic depressive disorders show wintertime exacerbation of symptoms as a seasonal overlay. Furthermore, a relatively small number of patients show both winter and summer depressive cycles, and are asymptomatic in fall and spring. Furthermore, many patients who meet criteria for seasonal pattern (winter type), show distinct slumps in mood and transient appearance of neurovegetative symptoms--short of meeting diagnostic criteria for severity and/or duration--during periods of bad weather during their normally asymptomatic seasons of the year.
In another variation, a similar clinical picture as found in winter depression may appear chronically, or intermittently but without seasonal pattern, given indoor environmental factors typical of the wintertime living and working environment. In one example, clinical observation shows that night shift workers, darkroom workers, and individuals who spend significant time in home or institutional environments with poor lighting are vulnerable to a light deprivation syndrome whose presentation is similar to that of winter depression. In another example, day workers at deficiently illuminated and ventilated work sites are vulnerable to a "sick building syndrome", which is characterized by atypical depressive symptoms above and beyond respiratory and digestive ailments presumably related to airborne pathogens.
It is estimated that about 10 million Americans suffer from winter depression at a fully syndromal level, with another 25 million suffering at a milder subsyndromal level which is less debilitating and may not meet diagnostic severity criteria. Prevalence estimates for nonseasonal atypical neurovegetative disorders are not yet known, but are thought to exceed that of disorders with seasonal pattern. Winter depression has been treated effectively with bright light therapy since it was first identified in the early 1980's, though the mechanism of action of light is still not well understood. The positive treatment effect, however, provides prima facie evidence that reduced daylight availability in fall and winter is a likely precipitant of the depressive episode. Indeed, the larger contraction of the natural photoperiod at more northerly latitudes is correlated with an increased prevalence of winter depression. Furthermore, patients with winter depression may show a sudden switch to hypomania shortly after initiation of light therapy, equal to or even exceeding the intensity of their summer episodes, in a light-dose-dependent manner. It is suspected that winter depression may also respond selectively to serotonergic antidepressants, although controlled trials are still largely lacking. Specific serotonin reuptake inhibitors are also known to serve as appetite suppressants. Therefore, it would be hypothesized that light itself activates serotonergic mechanisms.